Orthopaedics Flashcards
What is osteoporosis?
A quantitive reduction in bone mass (reduced overall bone density)
50 yr old Female pt comes in with neck if femur/distal radius/spine fracture (insufficiency fracture) after a low energy fall , progressive kyphosis, smoker with low BMI, poor intake of calcium and VitD, and hyperthyroidism. What is the diagnosis?
Osteoporosis
What are the investigations of osteoporosis?
DEXA scan (T score of -2.5) Investigations to rule out other causes of OP (TFTs)
How would you manage osteoporosis?
Prevention of bone loss and stimulation of bone regeneration
Bone loss inhibitors: bisphosphonates
Bone regenerators: oestrogen, calcium, vitamin D and strontium
What is rheumatoid arthritis?
A chronic, systemic inflammatory disease affecting the synovial joints and extra-articular system
A young female (30-50yrs), presents with insideous onset of generalised joint aches and stiffness, worse in the mornings. Her hands and feet are swollen, stiff and painful, and is the same on both sides (symmetrical). She is also experiencing fatigue, malaise and is of a low BMI. What is the diagnosis?
Rheumatoid Arthritis
RA symptoms are relapsing and remitting in different large joints, what is the sub-type?
Palindromic presentation
On examination of RA, what are the articular signs?
Small joint swelling Ulnar deviation, solar subluxation at MCPJs Boutonniere and swan neck deformities Z-thumbs Feet - claw toes and hallux valgus
What joint in RA, if subluxation occurs in, threatens the spinal cord?
Atlanto-axial joint
On examination of RA, what are the extra-articular signs?
Rheumatoid nodules
Osteoporosis (OP)
Carpal tunnel syndrome (multifocal neuropathies)Anaemia
Lymphadenopathy
Vasculitis
Pericarditis
Pulmonary fibrosis
Scleritis, berato conjunctivitis, sick syndrome
Amyloidosis
Felty’s syndrome (splenomegaly and neutropaenia)
ASSOCIATED: sjogre’s syndrome (autoimmune exocrinopathy)
In RA, what investigations would you send pt for? And what are the results/signs
Xray - periarticular erosions, soft tissue thickening, loss of joint space, sublimed or dislocated joints
Bloods - No test is specific - but Rheumatoid factor - +ve in 80%. Non-specific, may be positive in sjogren’s syndrome, SLE and sarcoid
Joint fluid assay - non specific but confirms inflammatory arthritis
Diagnostic criteria for RA
Morning stiffness (>1hr for >6weeks)
joint swelling
nodules
positive lab tests and radiographic findings
How do you manage RA? Non-surgically and surgically. What is the treatment goal?
Non-operative: exercise, physio and OT, orthoses
Medical - NSAIDS, antimalarials, disease modifying agents (methotrexate, sulfasalazine, gold and penicillamine), steroid injections, cytotoxic drugs, TNF- inhibitors (infliximab)
Surgically: (Aim to improve function and reduce pain)
synovectomy, soft tissue realignment, arthroplasty
Goal: control destructive synovitis, reduce pain, maintain joint function, prevent deformity - all in an MDT setting.
What is osteoarthritis?
A disorder of synovial joints characterised by focal articular cartilage degeneration, irregular regeneration and remodelling of subchondral bone
A 70+ yr old female, white European who is obese, presents with pain, stiffness and functional loss in her right hand. Initially, the pain was only on exercise, but has increased to being a ever present background pain, w/ exacerbations when in use. O/E tenderness and crepitations in wrist. Diagnosis and causes?
OA Causes: primary (idiopathic) secondary: biomechanics (instability) biochemical (Gaucher's disease congenital (DDH, epiphyseal dysplasia osteochondritides osteonecrosis crystal deposition
What is the pathophysiology of OA?
cartilage loss from an imbalance between synthesis and degradation
Differentials of OA
Monoarticular: acute trauma, septic arthritis, crystal synovitis
Polyarticular: reactive arthritis, inflammatory arthritis
Treatment of OA
Lifestyle changes: weight loss, exercise (for range of motion preservation and muscle strengthening), change in activity to avoid high load bearing activity
Cushioned footwear to reduce impact on lower limb joints
Sticks, crutches, splints
Analgesia and anti-inflammatories (NSAIDs as second line)
Surgery: Arthroplasty in knee and hip, also in ankle and shoulder
Arthrodesis in ankle and DIPJs of hand and foot, and spine
(Osteotomy, cartilage transplant and joint distraction have limited indications)
<50yr old male presents with nocturnal hip pain and joint irritability with slight effusion around the NOF joint following fall. PMH: sickle cell, SH: alcoholic.
What is the likely diagnosis? What investigations would you like to do and what will you see?
AVN (awn if adjacent to articular surface - overall aseptic bone necrosis)
Investigations: early changes seen on MRI
late changes on plain radiograph -> osteopenia and osteosclerosis, later subchondral fracture and collapse)
Causes of AVN/aseptic bone necrosis?
vascular micro emboli (sickle cell, haemaglobinopathies, decompression nitrogen emboli, fat emboli from pancreatitis) Mechanical interruption (trauma) Infection Drugs (corticosteroids, alcohol) Radiation / autoimmune vasculitis DM or Gaucher's disease
How would you treat AVN?
Remove avoidable RF
Offload joints to prevent collapse whilst healing occurs
Decompression of lesion by drilling or osteotomy
What are oteochondroses, their cause and give some common types?
Eponymous conditions characterised by degenerative changes or osteonecrosis followed by decalcification or regeneration.
Cause: traction of apophyses of immature skeleton, osteonecrosis with poor vascular supply and repeated micro trauma.
Groups:
Articular (joint space involved) - legs-calve perches disease
Monoarticular - osgood-schlatter (traction apophysitis of tibial tuberosity). Patella apophysitis = SLJ.
Epiphyseal - scheuermann;s (defect in secondary ossification of vertebrae)
What are the 3 different types of disorders of the matrix, and the disease examples of each?
Matrix deposition - osteogenesis imperfecta
Inadequate matrix resorption - Paget’s disease, osteoporosis
Insufficient matrix turnover - osteoporosis
pt, young pre pubescent presents with fragility fractures, short stature, blue sclera and dental problems. What is the diagnosis. What causes this? Give some other clinical features.
Osteogenesis imperfecta
An inherited defect in type 1 collagen synthesis.
Features: blue sclera, deafness, dentiogenesis imperfecta (teeth involvement), scoliosis, ligamentous laxity, basilar invagination causing spasticity and apnoeic spells.
Pt with osteogenesis imperfecta, what investigations would you like to carry out, and how would you manage the condition?
Radiology - shows slow generalised osteopenia with thin cortices and healing fractures of varying ages. Wormian bones seen on x-ray.
Management: protect child from fractures, immobilise bones as for normal fractures.
With multiple long bone fractures, use intramedullary rods with multiple osteotomies.
Severe scoliosis requires instrumental fusion as bracing is ineffective
50 year old man (from UK, USA/AUS) some signs of degenerative joint disease, bone pain, bowed tibia, high output cardiac failure. What is the diagnosis? Why is deafness a concern?
Paget’s disease
Cranial nerve compression from enlarged skull bones e.g VIII in petrous temporal bone causes deafness
What is paget’s disease and what what are they at risk from?
Metabolic bone disease of unknown aetiology, characterised by abnormal bone remodelling and greatly increased bone turnover. Results in coarse trabecular in weakened hyper vascular bone -> fracture prone
Risk of sarcomatous change - beware localised unrelenting pain and rapid x-ray progression or soft tissue mass
What investigations would you do and what would they show in Paget’s disease? How would this be managed?
Investigations
x-rays: bony expansion, remodelled bone, coarse trabeculae. Sclerotic and portico matrix - can mimic mets but they don’t usually expand bone.
Bone scan: increased uptake in affected bone. useful to determine mono or polyostotic.
Bloods: raised ALP
Urine: raised hydroxyproline indicates increased bone turnover
Management: analgesics for pain, bisphosphonates may reduce progression and hypervascularity. Osteotomy or joint replacement.
Hyperparathyroid, cushing’s and acromegaly are the three main endocrine cell disorders which affect bone. What bone abnormalities are associated with each?
Hyperparathyroid
primary - hypercalcaemia features: bone disease - browns tumours, fracture, osteopenia, deformity.
Cushing’s - OP, AVN of bone
Acromegaly - larger hands and feet, skull hypertrophy, hypercalcaemia
What are the 3 main bone minerals? What 3 hormones regulate them? What 3 organs do they act on?
Minerals: Calcium, phosphate and magnesium. Hormones: vitamin D, PTH, calcitonin
Organs: bone (mineral reservoir), intestine (dietary mineral absorption) and kidney (mineral excretion). This achieves homeostasis.
Pt presents with muscle weakness (proximal), bone pain, tiredness, enlarged joints (from metaphyseal swelling) and fractures. PMH: childhood rickets
Diagnosis and cause?
Osteomalacia - incomplete osteoid mineralisation following physeal closure (qualitative bone deficiency) *quantitative is osteopenia/porosis.
Causes: vitamin D/calcium/phosphorus deficiency; inadequate gut absorption; excessive excretion; genetic - vitD resistant rickets; drugs - phenytoin, phosphate-binding antacids, chronic alcoholism
You suspect a patient has osteomalacia, what investigations would you like to do? How would you manage them?
Bloods: calcium (low), phosphate (low), ALP (high in VitD deficient rickets, low in hypophosphatasia)
Urine: calcium. If FH of hypophophataemia, check for urinary phosphoethanolamine
X-rays: osteopenia, coarse trabeculae,
Treatment: usually involves dietary supplements
Pt presents with an infected joint. What signs and symptoms would they have and what is the likely causative organism?
presentation: pain (acute, constant), swelling, redness, warmth, loss of function, systemic fever
Most common cause of septic arthritis: s. aureus.
Others to consider: strep, H.Influeza (in children), N. gonorrhoea (if sexually active).
Investigations and management of a septic joint? Why does this need to be treated within 48 hrs. Complications to consider?
Ix:
Bloods: FBC, ESR, CRP, uric acid, cultures, clotting, rheumatoid immunology
X-ray: fracture? erosions, chondrocalcinosis
Joint aspiration: microscopy for crystals, culture and antibiotic sensitivities
Management: early washout, antibiotics - 2 week IV course usually, followed by 4 week oral.
Infection, proteolytic enzymes and loss of nutrition cause irreversible cartilage damage within 48 hrs
Complications: secondary osteoarthritis, recurrent infection
